tbuckley/cabot-search huggingface dataset:
Abstract 11427: Clot Strength and Platelet Reactivity for Prediction of Major Cardiovascular Events After Percutaneous Coronary Intervention
Authors: Osung Kwon, Jong-Hwa Ahn, Jin-sin Koh, Yongwhi Park, Seok-Jae Hwang, Sang-Wook Kim, Jinyong Hwang, Young-Hoon Jeong
Journal: Circulation (2022)

Introduction: Platelet-fibrin clot strength (PFCS) is associated with the risk of major adverse cardiovascular events (MACE) in patients with coronary artery disease (CAD). Hypothesis: The interaction between PFCS and platelet reactivity, and their prognostic implication remain uncertain. Methods: We enrolled CAD patients undergoing percutaneous coronary intervention (PCI) with available PFCS (measured by thromboelastography) and platelet reactivity (measured by VerifyNow). PFCS High was defined as maximal amplitude (MA)≥68, and high platelet reactivity (HPR) was categorized as P2Y12 reaction unit (PRU) &gt;208. Patients were stratified into 4 groups according to the levels of MA and PRU: (1) normal platelet reactivity (NPR)-PFCS Low (31.9%); (2) HPR-PFCS Low (28.9%); (3) NPR-PFCS High (18.1%); and (4) HPR-PFCS High (21.1%). The primary endpoint was MACE (a composite of all-cause death, myocardial infarction, or stroke) and the risk of major bleeding was also evaluated. Results: At 4-year follow-up, prognostic implication of HPR and PFCS High showed the synergistic effect, and risks of MACE were significantly different across the groups (log-rank test, P &lt; 0.001) (Figure 1). Compared with the NPR-PFCS Low group, the HPR-PFCS High group only showed a significantly higher risk of MACE (adjusted hazard ratio [HR adj ]: 1.87; 95% confidence interval [CI]: 1.22-2.87; p=0.004). In addition, the HPR-PFCS High group had a greater rate of MACE compared with the HPR-PFCS Low group (HR adj : 1.47; 95% CI: 1.04-2.09; p=0.03). Similar results were revealed in the risk of all-cause death. Compared with HPR-PFCS Low , NPR-PFCS Low was associated with a higher major bleeding rate (HR adj : 3.03; 95% CI: 1.27-7.14; p=0.01). Conclusions: In PCI-treated patients, PFCS and HPR phenotypes show important relationships in the occurrence of adverse clinical events. Therefore, a combined assessment of clot strength and platelet reactivity may enhance post-PCI risk stratification.
Abstract 12148: A New Perspective in the Management of Paroxysmal Atrial Fibrillation: Dual Anti-Arrhythmic Medications
Authors: Rana Al-zakhari, safa mousa, Nicholas Sheets, Edmund Appiah-Kubi, Philipa Owusu-Antwi, Ryan Isber, Nidal Isber
Journal: Circulation (2022)

Introduction: Atrial fibrillation is the most common disorder of cardiac rhythm, which is often associated with a high risk of morbidity and mortality. Antiarrhythmic medications (AAMs) continue to be the mainstay in the treatment of paroxysmal atrial fibrillation. However, the use of these medications has been limited by their modest anti-arrhythmic efficacy. Hypothesis: We hypothesized that dual AAMs (sodium/potassium channels blockers) improve the chance of maintaining sinus rhythm and decrease the need for catheter ablation when compared to single AAM. Methods: We conducted a retrospective observational study; we reviewed medical records of 150 patients with paroxysmal atrial fibrillation over five years at our hospital in New York. We collected the following data: age, sex, comorbidities, electrocardiogram findings, ejection fraction by echocardiography, classes of AAMs, duration and response to treatments. A successful response was defined as the absence of symptoms and the presence of sinus rhythm on electrocardiogram. A failed response was defined as persistence of symptoms and/or atrial fibrillation on electrocardiogram and the subsequent need for catheter ablation. Results: 86 patients met the inclusion criteria in our analysis. The average age of the patinets was 71.06 years. 45 patients were given the dual AAMs of either amiodarone+flecainide or dronedarone+flecainide, and were treated for an average of 15.4 months. 41 patients received a single AAM then catheter ablation if needed. A chi-square test was performed. X 2 =18.9429, p&lt;.0001. Patients taking dual AAMs were very likely to maintain sinus rhythm and less likely to need catheter ablation (Figure). Conclusions: Our preliminary results demonstrate that patients who receive dual AAMs are significantly less likely to need catheter ablation than those who receive single AAM. Well-designed prospective studies are needed to further explore the use of dual AAM therapy and its clinical impact.
Abstract 11130: Impact of Metabolic Surgery on Left Ventricular Structure and Function in Patients at High Risk for Heart Failure With Preserved Ejection Fraction
Authors: Diarmaid Hughes, Krishna Sanaka, Rickesha Wilson, Yoshihito Saijo, Nicholas Chan, Ashwin Kumar, Richard A Grimm, Brian P Griffin, Wai Hong Tang, Steven E Nissen, Ali Aminian, Bo Xu
Journal: Circulation (2022)

Introduction: Obesity is a major risk factor for HFpEF. Metabolic surgery has proven to be effective in reducing heart failure incidence. Hypothesis: This study examined the impact of metabolic surgery on LV structure and function in patients with high risk for HFpEF. Methods: Patients undergoing metabolic surgery between March 2005 and February 2019 with pre- and post-operative TTE imaging, a preserved EF (&gt;=50%) and a H 2 FPEF score &gt;=5 were recruited for this study. A H 2 FPEF score of ≥5 is considered a high possibility of HFpEF diagnosis. Results: Table 1 shows baseline characteristics of the 126 patients that met the entry requirements. The mean age was 65.5 years (SD 8.9) and 64.3% were female. Table 2 outlines the clinical and echocardiographic variables before and after metabolic surgery. There was a significant decrease in mean body mass index (BMI) post operatively, from 47.7 to 36.6 (P&lt;0.001), along with a number of statistically significant improvements in cardiovascular risk factors including a decrease in mean systolic blood pressure (BP) from 138 to 131 mmHg (P=0.005) and mean diastolic BP from 75 to 71 mmHg (P=0.014). There were improvements seen in the LV structure and function with the LV mass decreasing from 247.8 g to 220.7 g (P&lt;0.001), and both the mean septal wall (1.4 cm to 1.3cm, P&lt;0.001) and posterior wall (1.2 cm to 1.1 cm, P=0.007) thicknesses decreasing. There was also an improvement in the average LV global longitudinal strain (GLS) from -15.6 to -17.7% (P&lt;0.001). Conclusions: This study demonstrates that for patients at high risk of HFPEF, metabolic surgery was associated with improvements in LV structure and function, including LVGLS.
Abstract 12317: Improving Prenatal Detection of Heart Disease Scalable Composite Analysis of Six Fetal Cardiac Biometrics
Authors: Aneela Reddy, Sara Rizvi, Erin Chinn, Chinmayee Athalye, Anita J Moon-Grady, Rima Arnaout
Journal: Circulation (2022)

While prenatal congenital heart disease (CHD) screening has improved, accuracy remains as low as 30 percent. Standard fetal biometrics—cardiac axis (CA), cardiothoracic ratio (CTR), RV fractional area change (FAC), LV FAC, RA:LA area ratio, RV:LV area ratio—are available from screening imaging and can each aid in CHD screening, but can be cumbersome to measure. Combinations of biometrics may offer further utility but are challenging to integrate at the point of care. We tested whether using these biometrics in combination has utility in CHD screening (normal vs. abnormal). Further, we tested whether automatically predicted biometrics could function similarly to manually-labeled biometrics for this purpose. We included 105 fetal echocardiograms (20 normal, 85 abnormal across 12 different CHD lesions). We manually calculated the six biometrics above, performed dimensionality reduction using principal component analysis, and then clustered the resulting data by K-means. A previously developed deep learning model (Arnaout et al Nature 2021) was also used to automatically predict biometrics for normal, tetralogy of Fallot, and hypoplastic left heart syndrome hearts and plotted on the above cluster map. Optimal number of clusters was four, with RV:LV ratio and CTR as the most important features distinguishing clusters. Cluster 1 was predominantly normal hearts with cluster 2-4 largely abnormal hearts (Figure 1). The sensitivity and specificity for predicting abnormal hearts (e.g. CHD) was 86% and 75%, respectively. Model-predicted biometrics landed in the same clusters as the manually labeled lesions (Figure 1). To our knowledge, this is the first use of clustering to provide visualization of multiple fetal cardiac biometrics at once and reveal diagnostic utility. Once tested in screening ultrasounds on a larger scale, clustering of automated biometrics may be clinically useful at the screening point of care to augment scalable population-based screening.
Abstract 12218: Nationwide Trends in Subsequent Myocardial Infarction Hospitalizations and Mortality in Elderly Patients With Prior Myocardial Infarction and Associated Racial/Socioeconomic Disparities: A National Inpatient Sample Analysis
Authors: Akhil Jain, Samuel Edusa, Aditya Sharma, Rabia Naseem, Gurmannat SIngh Kang, Ibadat Anmol Singh, Aakash Desai, Yash Patel, Shilpa Reddy, Nafisa Reyaz, SAMIR STANIKZAI, Rupak Desai
Journal: Circulation (2022)

Background: There is a scarcity of large-scale data on race, sex, and economic status-based disparities in trends of subsequent/recurrent myocardial infarction (MI) in elderly individuals who have had a previous MI. Methods: National Inpatient Sample databases (2016-2019, ICD10 codes) were queried to identify elderly (≥65 years) patients with prior MI and divided into having and not having subsequent MI admissions. Primary outcomes were nationwide trends in subsequent MI admissions and all-cause in-hospital mortality in these patients with racial, sex, and economic status disparities. Results: A total of 421,960 recurrent MI admissions were identified [61.1% male, 38.9% female, 80.7% white and median age 76yrs (p&lt;0.001)]. Between 2016 and 2019, both males and females experienced an increase in recurrent MI from 9.1 to 10.6% and 8.1 to 9.8%, respectively, but a reassuring decrease in in-hospital mortality from 7.75 to 6.4% and 7.8 to 6.6% (P trends &lt;0.001). All race groups demonstrated a rise in recurrent MI, with blacks experiencing the largest increase from 9.2 to 11.7%(P trend &lt;0.001). In-hospital mortality for recurrent MI declined in all races except blacks and Native Americans (P trends &gt;0.05), with Asian/Pacific Islanders experiencing the highest decline from 13 to 7.4%(P trends &lt;0.001). All income quartile groups had an increase in recurrent MI with a more prominent increase in the lowermost income quartile cohort (P trends &lt;0.001). There was an overall trend of decreasing in-hospital mortality except for the lowermost income quartile which did not show improving trends in mortality (P trend =0.079). Conclusions: Elderly patients with a history of MI had an upward tendency for recurrent MI hospitalizations but a downward trend for all-cause in-hospital mortality with prevailing racial and socioeconomic disparities. Blacks and lower income quartile patients with CVD risk may need focused post-MI care to curtail subsequent MI and mortality risk.
Abstract 12293: Retinoic Acid Signaling Regulates Smooth Muscle Cell Phenotypic Switching in Atherosclerosis Through Epigenetic Modulation of Gene Expression
Authors: Huize Pan, Chenyi Xue, Jian Cui, Leila S Ross, Sebastian E Ho, Muredach P Reilly
Journal: Circulation (2022)

Background: Smooth muscle cells (SMCs) substantially contribute to atherosclerosis through “phenotypic switching.” Our previous work identified an intermediate SMC-derived cell type, termed “SEM” cells, which was multipotent and activated in inflammatory response. Activation of retinoic acid (RA) signaling by all-trans retinoic acid (ATRA) attenuated atherosclerosis in mice coincident with dramatic suppression of SEM cell formation from SMCs. However, the regulatory mechanisms by which RA signaling modulates SMC transition to SEM cells are largely unknown. Methods: We employed molecular and cell biology techniques, SMC-linage tracing and atheroprone mouse models, and next-generation sequencing (e.g., RNA-seq, ChIP-seq) to reveal how RA signaling modulates SMC transition to SEM cells. Results: Activation of RA signaling with ATRA significantly reduced SEM cells in established atherosclerosis, as well as downregulated the expression of SEM cell marker genes (e.g., Ly6a , Ly6c1 ) and repressed inflammatory response in ex vivo SEM cells, whereas inhibition of the signaling with antagonist, BMS49334, showed opposite results. RARα occupied the promoter regions of SEM cell marker genes, and ATRA treatment significantly increased the enrichment of NCOR1 at promoters of these genes. These findings suggest that RA signaling suppresses SMC transition to SEM cells via directly repressing the expression of SEM cell marker genes. Furthermore, we found EZH2, one of the subunits of PRC2, physically interacted with RARα in SMCs and occupied the promoters of SEM cell marker genes, and its methyltransferase activity at the promoter regions was responsible for the repression of SEM cell maker genes. Moreover, activation of RA signaling inhibited SEM cell inflammatory response through LXR-mediated suppression of a series of inflammatory genes. Finally, multiple epigenetic signatures (e.g., H3K27me3, H3K27ac, H3K4me3, etc.) at TSS of SEM cell marker genes and inflammatory genes were extensively altered in response to the activation of RA signaling. Conclusions: Our findings indicate that RA signaling modulates maintenance of SEM cell identity and inflammatory function in atherosclerosis by epigenetic regulation of gene expression.
Abstract 12411: Validation of Academic Research Consortium for High Bleeding Risk (ARC-HBR) Definition in East-Asian Patients
Authors: Jinho Lee, Min-ju Kim, Mijin Kim, Jinsun Park, Hoyun Kim, Cho Suji, Choi Yeonwoo, Junghoon Lee, Ju Hyeon Kim, Cha Sung Joo, Taeoh Kim, Doyoon Kang, Pil Hyung Lee, Jung-Min Ahn, Seung-jung Park, Dukwoo Park
Journal: Circulation (2022)

Introduction: Clinical applicability of the Academic Research Consortium High Bleeding Risk (ARC-HBR) criteria in East-Asian patients receiving potent antiplatelet therapy for acute coronary syndromes (ACS) is still undetermined Methods: Using individual patient data from the TICAKOREA trial, which is a multicenter trial randomly compared ticagrelor and clopidogrel in Korean patients with ACS, we determined the prognostic effect of ARC-HBR criteria on bleeding and ischemic events. The primary safety outcome was bleeding of academic research consortium (BARC) type 3 or 5 and primary efficacy outcome was major adverse cardiovascular events (MACE; a composite of cardiovascular death, myocardial infarction, or stroke). Results: HBR patients compared with non-HBR patients had a higher incidence of BARC type 3 or 5 bleeding (10.0% vs. 3.61%; hazard ratio [HR], 2.98; 95% confidence interval [CI], 1.52 to 5.86) and MACE (14.3% vs. 6.1%; HR 2.35; 95% CI, 1.35-4.10). Among HBR patients, there was no significant difference in bleeding events between ticagrelor and clopidogrel (10.2% vs. 9.8%; HR 1.15; 95% CI, 0.38-3.44). However, the efficacy endpoint of MACE tended to be higher in the ticagrelor group than in the clopidogrel group (19.1% vs. 8.1%; HR 2.31; 95% CI, 0.91-5.83) Conclusions: In Korean patients with ACS intended to receive early invasive management, ARC-HBR criteria is sufficiently applicable to predict both bleeding and ischemic risk. We also observed differential safety and effectiveness of ticagrelor compared with clopidogrel according to presence or absence of ARC-HBR criteria.
Abstract 12026: A Case of Eosinophilic Endomyocarditis in a Patient With Eosinophilic Leukemia and Hypereosinophilic Syndrome
Authors: Navjot Singh, Ravi J Shah, DHRUBAJYOTI BANDYOPADHYAY, Akshay Goel, Joseph Harburger, Pragya Ranjan
Journal: Circulation (2022)

Background: Eosinophilic (Loeffler’s) endomyocarditis is a restrictive cardiomyopathy caused by eosinophilic infiltration of myocardial. Complications include arrhythmias, intraventricular thrombus formation, and acute heart failure. Clinical Presentation A 37-year-old man with no past medical history presented with two weeks of fatigue and exertional dyspnea. He was found to have acute eosinophilic leukemia with a total white blood cell count of 440 k/mm^3 with 14% myelocytes, hypereosinophilic syndrome with an absolute eosinophil count of 56 k/mm^3, severe anemia and thrombocytopenia. Bone marrow biopsy and peripheral blood FISH analysis confirmed eosinophilic leukemia. He subsequently underwent leukopheresis, followed by treatment with hydroxyurea and imatinib. Cardiac Evaluation Echocardiogram revealed endomyocardial thickening of the left ventricular apex (Figure 1A). Cardiac MRI revealed left ventricular apical subendocardial wall thickness of 16 mm with subendocardial late gadolinium enhancement consistent with endomyocardial fibrosis (Figure 1B). The average global T1 value was 1100 ms and the calculated extracellular volume was 35%. MRI also revealed an apical left ventricular thrombus. The patient was treated with pulse dose of steroids in addition to the cancer-specific regimen. He did not initially receive anticoagulation due to severe anemia and thrombocytopenia. Subsequent echocardiography after three months of treatment revealed complete resolution of endomyocardial thickening and no evidence of a left ventricular thrombus. He had resolution of peripheral leukocytosis, hypereosinophilia, anemia, and thrombocytopenia. Conclusion This case presents the diagnosis and multidisciplinary management of eosinophilic endomyocarditis related to eosinophilic leukemia. Complete clinical and echocardiographic resolution was achieve following treatment with pulse-dose steroids and a cancer-specific regimen.
Abstract 11546: Racial Disparities in Zip-Code Level Social Determinants of Health and Cardiovascular Outcomes in Females With Breast Cancer
Authors: Nickolas Stabellini, Mantas Dmukauskas, Jennifer Cullen, Amie J Barda, Lifen Cao, Justin Moore, Susan F Dent, John Shanahan, Nelson Hamerschlak, Jill Barnholtz-Sloan, Kristin Waite, Alberto Montero, Avirup Guha
Journal: Circulation (2022)

Introduction: Cardiovascular disease (CVD) prevalence and cancer mortality are higher in non-Hispanic Blacks (NHB) relative to other racial subpopulations. Hypothesis: Among females with BC (≥18 years), there are racial differences in cardiac events (CEV) which can be explained by adverse social determinants of health (SDOH). Methods: Data were obtained from a Cleveland area integrated health care systems informatics platform. (2005-2019). Zip-code level demographic features were extracted using the SDOH Database from the Agency for Healthcare Research and Quality. The CEVs included were heart failure (HF), acute coronary syndrome (ACS), and ischemic stroke (IS). Multivariable Cox proportional hazards regression models were used to examine racial disparities in CEVs. Race-stratified (NHB and non-Hispanic Whites [NHW]) multivariable logistic regression was performed to assess the role of each SDOH in association with CEV. Results: This study included 9,022 females with breast cancer (BC) of which 18.8% were NHB, and 48.7% had a CEV. The racial differences in CEV and the role of zip-code level SDOH are presented in Table 1. These racial differences were not explained by the proportion of people unemployed in the zip code (p=0.42, race*unemployment % [cross-product]), proportional of people in the zip code with only a high school diploma (p=0.66, race*education % [cross-product]), and proportion of people in the zip code who use public transport (p=0.24, race * transport % [cross-product]). Conclusion: There are racial differences in the risk of ACS and IS after a BC diagnosis, but this does not seem to be explained by the 3 adverse zip-code level SDOH included in this study. Therefore, studies with individual-level SDOH and including other domains are necessary to better understand their relationship with CEVs.
Abstract 12547: Obesity as Risk Factor for Malignant Ventricular Arrhythmias in Phospholamban Cardiomyopathy
Authors: Belend Mahmoud, Remco de Brouwer, Myrthe Y van der Heide, Tom E Verstraelen, Arthur A Wilde, Carol Ann Remme, Diederik W Kuster, Paul A Van Der Zwaag, Herman H Sillje, Maarten P van den Berg, Dirk J van Veldhuisen, Moniek G Cox, B D Westenbrink, Rudolf A De Boer
Journal: Circulation (2022)

Introduction: The pathogenic phospholamban (PLN) p.Arg14del mutation can cause severe arrhythmogenic cardiomyopathy. However, disease penetrance and clinical course are heterogenous and can differ largely between affected individuals. The impact of external factors - such as lifestyle - on the clinical course has not been studied yet. Hypothesis: We hypothesized that obese PLN mutation carriers have worse clinical outcomes, characterized by a higher burden of malignant ventricular arrhythmias (MVA). Methods: PLN p.Arg14del mutation carriers from the Dutch PLN registry with available follow-up (FU) data were included. MVA was defined as either sustained ventricular tachycardia, ventricular fibrillation, appropriate implantable cardioverter defibrillator intervention or (aborted) cardiac arrest. Patients were categorized into three groups based on their body mass index (BMI): normal weight (BMI 18.5 - 24.9 kg/m 2 ), overweight (25.0 - 29.9 kg/m 2 ) and obese (BMI &gt; 30.0 kg/m 2 ). Mutation carriers with a BMI &lt; 18.5 kg/m 2 or MVA at baseline were excluded. Results: A total of 179 PLN mutation carriers were included in this analysis: 105 (58.7%) normal weight, 59 (33.0%) overweight, 15 (8.4%) obese. The obese group had the highest percentage of MVA (26.7%), followed by the overweight (13.6%) and normal weight (4.8%) groups, as shown in the Kaplan-Meier curve (log-rank 0.016). Continuous BMI was significantly correlated with the incidence of MVA during FU: hazard ratio 1.15 [1.04 - 1.27; p=0.006] per 1-unit increase of BMI, adjusted for age, sex and comorbidities (hypertension, type 2 diabetes mellitus, dyslipidemia, coronary heart disease). Additionally, BMI value predicted MVA with an area under the curve of 0.73 [0.63 - 0.84; p=0.002]. Conclusions: In PLN p.Arg14del mutation carriers, high BMI values and obesity are associated with higher incidence of MVA. This suggests a potential role for lifestyle intervention in the management of this genetic cardiomyopathy.